scholarly journals Buffer Therapy in Acute Metabolic Acidosis: Effects on Acid-Base Status and Glomerular Permeability

2019 ◽  
Author(s):  
Jan Schnapauff ◽  
David Piros ◽  
Anna Rippe ◽  
Peter Bentzer ◽  
Naomi Clyne ◽  
...  
Keyword(s):  
Metabolic Acidosis ◽  
Extracellular Fluid ◽  
Strong Ion Difference ◽  
Acid Base ◽  
Glomerular Permeability ◽  
Filtration Barrier ◽  
Bicarbonate Therapy ◽  
Acid Base Status ◽  
Acute Metabolic Acidosis ◽  
Cellular Components

ABSTRACTBackground:Correction of acute metabolic acidosis using sodium bicarbonate is effective, but has been hypothesized to exacerbate intra-cellular acidosis causing cellular dysfunction. The effects of acidemia and bicarbonate therapy on the cellular components of the glomerular filtration barrier, crucial for the integrity of the renal filter, are as yet unknown. Controversy persists regarding the most appropriate method to assess acid-base status: the “Stewart approach” or the “Siggaard-Andersen approach” using the standard base excess (SBE).Methods:Here we performed physiological studies in anesthetized Sprague-Dawley rats during severe metabolic acidosis (HCl iv 6 mmol kg-1) and following bicarbonate (2.5 mmol kg-1) administration. We assessed glomerular permeability using sieving coefficients of polydisperse fluorescein isothiocyanate (FITC)-Ficoll 70/400. Acid-base status was evaluated using SBE, standard bicarbonate, total CO2, the Stewart-Fencl strong ion difference (ΔSID = Na – Cl – 38) and a theoretical model of plasma and erythrocyte strong ion difference.Results:Our data show that neither acidosis nor its correction with NaHCO3altered glomerular permeability. We identified ΔSID as a strong estimator of plasma base excess (as assessed using the Van Slyke equation).In silicomodeling indicates that changes in the strong ion difference in erythrocytes would explain their buffering effect by means of a shift of anions from the extracellular fluid.Conclusion:These data demonstrate a remarkable tolerance of the glomerular filter to severe acute acidosis and bicarbonate therapy. Our results also cast light on the buffer mechanism in erythrocytes and the ability of different acid-base parameters to evaluate the extent of an acid-base disorder.IMPORTANCE STATEMENTMetabolic acidosis is a frequent complication of acute kidney injury in critically ill patients and is associated with a high risk of mortality. Correction of acidosis using sodium bicarbonate is simple and effective, but could possibly induce intracellular acidosis causing cellular dysfunction. The effects of acidemia and subsequent bicarbonate treatment on the cellular components of the glomerular filtration barrier, crucial for the integrity of the renal filter, are unknown. We show that neither severe acidemia nor bicarbonate therapy appear to have negative effects on glomerular permeability. Our analysis also highlights the buffering effects of erythrocytes, which appear to be mediated by a shift of strong anions into the red cells, increasing the strong ion difference in the extracellular fluid.

Evaluation of bicarbonate transport in rat distal tubule: effects of acid-base status

1982 ◽  
Vol 243 (4) ◽  
pp. F335-F341 ◽  
Author(s):  
M. S. Lucci ◽  
L. R. Pucacco ◽  
N. W. Carter ◽  
T. D. DuBose
Keyword(s):  
Metabolic Acidosis ◽  
Respiratory Acidosis ◽  
Distal Tubule ◽  
Bicarbonate Transport ◽  
Acid Base Balance ◽  
Acid Base ◽  
Bicarbonate Reabsorption ◽  
Base Balance ◽  
Acid Base Status ◽  
Acute Metabolic Acidosis

Previous micropuncture studies utilizing indirect methods to estimate bicarbonate transport in the rat superficial distal tubule have indicated that the distal bicarbonate reabsorptive process normally operates well below the saturation level. Recent studies from our laboratory failed to demonstrate a spontaneous acid disequilibrium pH in this segment, implying that the bicarbonate reabsorptive rate was less than previously estimated. The purpose of the present experiments were 1) to measure the rate of absolute bicarbonate reabsorption by the rat superficial distal tubule while controlling bicarbonate delivery, and 2) to examine the effects of alterations in acid-base status on the rate of bicarbonate reabsorption. Five groups of rats in different states of acid-base balance were studied. No significant bicarbonate reabsorption was detected in the control hydropenic, combined respiratory acidosis-metabolic alkalosis, acute respiratory acidosis, or acute metabolic acidosis groups. In contrast, metabolic acidosis of 3 days duration resulted in a significant bicarbonate reabsorptive rate of 52.6 +/- 13.9 pmol . mm-1 . min-1. The observation of significant bicarbonate reabsorption in the distal tubule only during chronic metabolic acidosis of 3 days duration is compatible with adaptation of this normally low-capacity segment to chronic changes in systemic acid-base states.

scholarly journals Chloride content of solutions used for regional citrate anticoagulation might be responsible for blunting correction of metabolic acidosis during continuous veno-venous hemofiltration

2016 ◽  
Vol 17 (1) ◽  
Author(s):  
Rita Jacobs ◽  
Patrick M. Honore ◽  
Marc Diltoer ◽  
Herbert D. Spapen
Keyword(s):  
Metabolic Acidosis ◽  
Chloride Content ◽  
Regional Citrate Anticoagulation ◽  
Strong Ion Difference ◽  
Strong Ion Gap ◽  
Acid Base ◽  
Citrate Anticoagulation ◽  
Acid Base Equilibrium ◽  
Acid Base Status ◽  
Regional Anticoagulation

Abstract Background Citrate, the currently preferred anticoagulant for continuous veno-venous hemofiltration (CVVH), may influence acid-base equilibrium. Methods The effect of 2 different citrate solutions on acid-base status was assessed according to the Stewart-Figge approach in two consecutive cohorts of critically ill adult patients. The first group received Prismocitrate 10/2 (PC10/2; 10 mmol citrate/L). The next group was treated with Prismocitrate 18/0 (PC18; 18 mmol citrate/L). Both groups received bicarbonate-buffered fluids in post-dilution. Results At similar citrate flow, the metabolic acidosis present at baseline in both groups was significantly attenuated in PC18 patients but persisted in PC10/2 patients after 24 h of treatment (median pH 7,42 vs 7,28; p = 0.0001). Acidosis in the PC10/2 group was associated with a decreased strong ion difference and an increased strong ion gap (respectively 43 vs. 51 mmol/L and 17 vs. 12 mmol/L, PC10/2 vs. PC18; both p = 0.001). Chloride flow was higher in PC10/2 than in PC18 subjects (25.9 vs 14.3 mmol/L blood; p < 0.05). Conclusion Correction of acidosis was blunted in patients who received 10 mmol citrate/L as regional anticoagulation during CVVH. This could be explained by differences in chloride flow between the applied citrate solutions inducing hyperchloremic acidosis.

scholarly journals Acid-Base Effects of a Bicarbonate-Balanced Priming Fluid during Cardiopulmonary Bypass: Comparison with Plasma-Lyte 148. A Randomised Single-Blinded Study

2008 ◽  
Vol 36 (6) ◽  
pp. 822-829 ◽  
Author(s):  
T. J. Morgan ◽  
G Power ◽  
B. Venkatesh ◽  
M. A. Jones
Keyword(s):  
Metabolic Acidosis ◽  
Cardiopulmonary Bypass ◽  
Base Excess ◽  
Strong Ion Difference ◽  
Acid Base ◽  
Elective Cardiac Surgery ◽  
Standard Base Excess ◽  
Acid Base Status ◽  
Standard Base ◽  
Normal Acid

Fluid-induced metabolic acidosis can be harmful and can complicate cardiopulmonary bypass. In an attempt to prevent this disturbance, we designed a bicarbonate-based crystalloid circuit prime balanced on physico-chemical principles with a strong ion difference of 24 mEq/l and compared its acid-base effects with those of Plasma-Lyte 148, a multiple electrolyte replacement solution containing acetate plus gluconate totalling 50 mEq/l. Twenty patients with normal acid-base status undergoing elective cardiac surgery were randomised 1:1 to a 2 litre prime of either bicarbonate-balanced fluid or Plasma-Lyte 148. With the trial fluid, metabolic acid-base status was normal following bypass initiation (standard base excess 0.1 (1.3) mEq/l, mean, SD), whereas Plasma-Lyte 148 produced a slight metabolic acidosis (standard base excess -2.2 (2.1) mEq/l). Estimated group difference after baseline adjustment was 3.6 mEq/l (95% confidence interval 2.1 to 5.1 mEq/l, P=0.0001). By late bypass, mean standard base excess in both groups was normal (0.8 (2.2) mEq/l vs. -0.8 (1.3) mEq/l, P=0.5). Strong ion gap values were unaltered with the trial fluid, but with Plasma-Lyte 148 increased significantly on bypass initiation (15.2 (2.5) mEq/l vs. 2.5 (1.5) mEq/l, P <0.0001), remaining elevated in late bypass (8.4 (3.4) mEq/l vs. 5.8 (2.4) mEq/l, P <0.05). We conclude that a bicarbonate-based crystalloid with a strong ion difference of 24 mEq/l is balanced for cardiopulmonary bypass in patients with normal acid-base status, whereas Plasma-Lyte 148 triggers a surge of unmeasured anions, persisting throughout bypass. These are likely to be gluconate and/or acetate. Whether surges of exogenous anions during bypass can be harmful requires further study.

scholarly journals Acid-base status in canine babesiosis caused by Babesia canis

2020 ◽  
Vol 90 (6) ◽  
pp. 603-610
Author(s):  
Marin Torti ◽  
◽  
Josipa Kuleš ◽  
Vesna Matijatko ◽  
Mirna Brkljačić ◽  
...  
Keyword(s):  
Metabolic Acidosis ◽  
Metabolic Alkalosis ◽  
Strong Ion Difference ◽  
Canine Babesiosis ◽  
Acid Base ◽  
Mixed Acid ◽  
Naturally Occurring ◽  
Base Disorder ◽  
Acid Base Status ◽  
Healthy Dogs

Acid-base disturbances have been reported in severe canine babesiosis caused by Babesia rossi (B. rossi), but they have not been studied in babesiosis caused by B. canis. The objective of this study was to determine the acid-base status, blood gases and electrolyte concentrations in naturally occurring canine babesiosis caused by B. canis, and to compare the results to those in healthy dogs. Two groups of animals were used: group 1 consisted of 10 healthy dogs, and group 2 consisted of 14 dogs naturally infected with B. canis. The following acid-base disturbances occurred in the dogs with naturally occurring babesiosis: half of the dogs had a mixed acid-base disorder, and the other half a simple acid-base disorder. The most common mixed disorder was metabolic acidosis with metabolic alkalosis. It may be said that a variety of acid-base disorders occurs in canine babesiosis. The dogs in the present study had metabolic acidosis due to hyperlactemia and hyperchloremia, metabolic alkalosis due to hypochloremia and hypoalbuminemia, and respiratory alkalosis due to hypoxemia. With the use of the strong-ion difference approach clearer recognition of mixed acid-base disorders and their better understanding is possible.

Changes in brain ECF pH during metabolic acidosis and alkalosis: a microelectrode study

1983 ◽  
Vol 55 (6) ◽  
pp. 1849-1853 ◽  
Author(s):  
S. Javaheri ◽  
A. De Hemptinne ◽  
B. Vanheel ◽  
I. Leusen
Keyword(s):  
Cerebrospinal Fluid ◽  
Metabolic Acidosis ◽  
Metabolic Alkalosis ◽  
Extracellular Fluid ◽  
Acid Base ◽  
Brain Extracellular Fluid ◽  
Group I ◽  
Venous Pco2 ◽  
Anesthetized Dogs ◽  
Acute Metabolic Acidosis

We used pH-sensitive double-barreled microelectrodes to measure brain extracellular fluid (ECF) pH in anesthetized dogs during isocapnic infusion acidosis (HCl) and alkalosis (Na2CO3) of 45-60 min duration. The diameter of the tips of these electrodes varied from less than 1 to 27 micron and were placed 5 mm below the surface of the parietal cortex. In group I (metabolic acidosis, n = 5) mean plasma and brain ECF pH fell significantly by 0.221 and 0.025, respectively, with changes in brain ECF pH being 11.3% of those noted in plasma. In group II (metabolic alkalosis, n = 5) mean plasma and brain ECF pH rose significantly by 0.170 and 0.049, respectively, with changes in brain ECF pH being 28.8% of those noted in plasma. Mean arterial and sagittal venous PCO2 and cisternal cerebrospinal fluid (CSF) acid-base variables did not change significantly during acid or base infusion. We conclude that during transients of isocapnic metabolic acid-base perturbations ionic gradients exist between brain ECF and CSF and that changes in brain ECF pH measured by microelectrodes follow the changes in plasma pH. These pH changes may play an important role in respiratory adaptations of acute metabolic acidosis and alkalosis.

scholarly journals Sodium Bicarbonate Therapy in Patients with Metabolic Acidosis

2014 ◽  
Vol 2014 ◽  
pp. 1-13 ◽  
Author(s):  
María M. Adeva-Andany ◽  
Carlos Fernández-Fernández ◽  
David Mouriño-Bayolo ◽  
Elvira Castro-Quintela ◽  
Alberto Domínguez-Montero
Keyword(s):  
Chronic Kidney Disease ◽  
Metabolic Acidosis ◽  
Kidney Disease ◽  
Sodium Bicarbonate ◽  
Negative Impact ◽  
Qtc Interval ◽  
Bicarbonate Therapy ◽  
Proximal Tubular ◽  
Acute Metabolic Acidosis ◽  
Renal Proximal Tubular

Metabolic acidosis occurs when a relative accumulation of plasma anions in excess of cations reduces plasma pH. Replacement of sodium bicarbonate to patients with sodium bicarbonate loss due to diarrhea or renal proximal tubular acidosis is useful, but there is no definite evidence that sodium bicarbonate administration to patients with acute metabolic acidosis, including diabetic ketoacidosis, lactic acidosis, septic shock, intraoperative metabolic acidosis, or cardiac arrest, is beneficial regarding clinical outcomes or mortality rate. Patients with advanced chronic kidney disease usually show metabolic acidosis due to increased unmeasured anions and hyperchloremia. It has been suggested that metabolic acidosis might have a negative impact on progression of kidney dysfunction and that sodium bicarbonate administration might attenuate this effect, but further evaluation is required to validate such a renoprotective strategy. Sodium bicarbonate is the predominant buffer used in dialysis fluids and patients on maintenance dialysis are subjected to a load of sodium bicarbonate during the sessions, suffering a transient metabolic alkalosis of variable severity. Side effects associated with sodium bicarbonate therapy include hypercapnia, hypokalemia, ionized hypocalcemia, and QTc interval prolongation. The potential impact of regular sodium bicarbonate therapy on worsening vascular calcifications in patients with chronic kidney disease has been insufficiently investigated.

Studies on the Pathophysiology of Encephalopathy in Reye's Syndrome: Hyperammonemia in Reye's Syndrome

PEDIATRICS ◽  
1975 ◽  
Vol 56 (6) ◽  
pp. 999-1004
Author(s):  
Daniel C. Shannon ◽  
Robert De Long ◽  
Barry Bercu ◽  
Thomas Glick ◽  
John T. Herrin ◽  
...  
Keyword(s):  
Metabolic Acidosis ◽  
Venous Drainage ◽  
Respiratory Alkalosis ◽  
Ammonia Concentration ◽  
Reye's Syndrome ◽  
Acid Base ◽  
Arterial Blood ◽  
Cerebral Venous Drainage ◽  
Acid Base Status ◽  
The Brain

The initial acid-base status of eight survivors of Reye's syndrome was characterized by acute respiratory alkalosis (Pco2=32 mm Hg; Hco3-= 22.0 mEq/liter) while that of eight children who died was associated with metabolic acidosis as well (HCO3-=10.0 mEq/liter). Arterialinternal jugular venous ammonia concentration differences on day 1 (299 mg/100 ml) and day 2 (90 mg/ 100 ml) reflected cerebral uptake of ammonia while those on days 3 and 4 (-43 and -55 mg/100 ml) demonstrated cerebral release. Arterial blood hyperammonemia can be detoxified safely in the brain as long as the levels do not exceed approximately 300µg/100 ml. Beyond that level lactic acidosis is observed, particularly in cerebral venous drainage. Arterial blood hyperammonemia was also related to the extent of alveolar hyperventilation. These findings are very similar to those seen in experimental hyperammonemia and support the concept that neurotoxicity in children with Reye's syndrome is at least partly due to impaired oxidative metabolism secondary to hyperammonemia.

Bicarbonate Therapy and Intracellular Acidosis

1997 ◽  
Vol 93 (6) ◽  
pp. 593-598 ◽  
Author(s):  
D. J. A. Goldsmith ◽  
L. G. Forni ◽  
P. J. Hilton
Keyword(s):  
Carbon Dioxide ◽  
Metabolic Acidosis ◽  
Sodium Bicarbonate ◽  
Intracellular Ph ◽  
Extracellular Fluid ◽  
Intracellular Acidification ◽  
Intracellular Acidosis ◽  
Bicarbonate Therapy ◽  
Intracellular Alkalinization

1. The correction of metabolic acidosis with sodium bicarbonate remains controversial. Experiments in vitro have suggested possible deleterious effects after alkalinization of the extracellular fluid. Disequilibrium of carbon dioxide and bicarbonate across cell membranes after alkali administration, leading to the phenomenon of ‘paradoxical’ intracellular acidosis, has been held responsible for some of these adverse effects. 2. Changes in intracellular pH in suspensions of leucocytes from healthy volunteers were monitored using a fluorescent intracellular dye. The effect in vitro of increasing extracellular pH with sodium bicarbonate was studied at different sodium bicarbonate concentrations. Lactic acid and propionic acid were added to the extracellular buffer to mimic conditions of metabolic acidosis. 3. The addition of a large bolus of sodium bicarbonate caused intracellular acidification as has been observed previously. The extent of the intracellular acidosis was dependent on several factors, being most evident at higher starting intracellular pH. When sodium bicarbonate was added as a series of small boluses the reduction in intracellular pH was small. Under conditions of initial acidosis this was rapidly followed by intracellular alkalinization. 4. Although intracellular acidification occurs after addition of sodium bicarbonate to a suspension of human leucocytes in vitro, the effect is minimal when the conditions approximate those seen in clinical practice. We suggest that the observed small and transient lowering of intracellular pH is insufficient grounds in itself to abandon the use of sodium bicarbonate in human acidosis.

Pendrin in the mouse kidney is primarily regulated by Cl− excretion but also by systemic metabolic acidosis

2008 ◽  
Vol 295 (6) ◽  
pp. C1658-C1667 ◽  
Author(s):  
Patricia Hafner ◽  
Rosa Grimaldi ◽  
Paola Capuano ◽  
Giovambattista Capasso ◽  
Carsten A. Wagner
Keyword(s):  
Metabolic Acidosis ◽  
Collecting Duct ◽  
Relative Number ◽  
High Protein ◽  
Acid Excretion ◽  
Acid Base ◽  
Urinary Acidification ◽  
Apical Side ◽  
Acid Base Status ◽  
Net Acid Excretion

The Cl−/anion exchanger pendrin (SLC26A4) is expressed on the apical side of renal non-type A intercalated cells. The abundance of pendrin is reduced during metabolic acidosis induced by oral NH4Cl loading. More recently, it has been shown that pendrin expression is increased during conditions associated with decreased urinary Cl− excretion and decreased upon Cl− loading. Hence, it is unclear if pendrin regulation during NH4Cl-induced acidosis is primarily due the Cl− load or acidosis. Therefore, we treated mice to increase urinary acidification, induce metabolic acidosis, or provide an oral Cl− load and examined the systemic acid-base status, urinary acidification, urinary Cl− excretion, and pendrin abundance in the kidney. NaCl or NH4Cl increased urinary Cl− excretion, whereas (NH4)2SO4, Na2SO4, and acetazolamide treatments decreased urinary Cl− excretion. NH4Cl, (NH4)2SO4, and acetazolamide caused metabolic acidosis and stimulated urinary net acid excretion. Pendrin expression was reduced under NaCl, NH4Cl, and (NH4)2SO4 loading and increased with the other treatments. (NH4)2SO4 and acetazolamide treatments reduced the relative number of pendrin-expressing cells in the collecting duct. In a second series, animals were kept for 1 and 2 wk on a low-protein (20%) diet or a high-protein (50%) diet. The high-protein diet slightly increased urinary Cl− excretion and strongly stimulated net acid excretion but did not alter pendrin expression. Thus, pendrin expression is primarily correlated with urinary Cl− excretion but not blood Cl−. However, metabolic acidosis caused by acetazolamide or (NH4)2SO4 loading prevented the increase or even reduced pendrin expression despite low urinary Cl− excretion, suggesting an independent regulation by acid-base status.

Plasma, Extracellular and Muscle Electrolyte Responses to Acute Metabolic Acidosis

1956 ◽  
Vol 186 (1) ◽  
pp. 131-138 ◽  
Author(s):  
Richard B. Tobin
Keyword(s):  
Metabolic Acidosis ◽  
Hydrochloric Acid ◽  
Intracellular Ph ◽  
Extracellular Ph ◽  
Acid Base ◽  
Extracellular Acidosis ◽  
Acid Load ◽  
Acute Metabolic Acidosis ◽  
Volumes Of Distribution

Nephrectomized cats were infused with hydrochloric acid in loads of from 3.5–9.6 mEq/kg. Extracellular moderation of the acidosis calculated from concentrations of electrolytes in plasma and inulin volumes of distribution was proportioned as follows: 35% by Na and 5% by K entering the ECS, and 20% by Cl and 24% by CO2 leaving the ECS. Calculated from changes in the chloride spaces, Na shift moderated 58%, CO2 22% and K 6% of the acid load. Sodium rather than potassium appeared to be the main extracellular moderator of acidosis under the conditions of these experiments. Direct muscle analyses showed a fall in intracellular Na and probably of K in response to extracellular acidosis. It is suggested that K i is not inversely related to extracellular ph. Calculated intracellular ph remained constant during the acidosis, indicating that cells may maintain a constant acid-base environment despite marked fluctuations of extracellular ph and that unmeasured mechanisms are responsible.

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